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. 2024 Jun 12;137(14):1651–1662. doi: 10.1097/CM9.0000000000003169

Figure 2.

Figure 2

The molecular mechanism of reduced sensitivity to ferroptosis in RA-FLS. Ferroptosis is mainly caused by iron-dependent lipid peroxidation. GPX4 is a crucial factor that inhibits ferroptosis. Decreasing the accumulation of LIP, activating of GPX4 or related signaling pathways can suppress lipid peroxidation production and prevent ferroptosis. RSL3 is a known ferroptosis inducer. The data cut-off date for the analysis was February 1, 2024. 4E-BP1: 4E binding protein 1; AKT: Protein kinase B; FLS: Fibroblast-like synoviocyte; FTH1: Ferritin heavy polypeptide 1; GPX4: Glutathione peroxidase 4; GSH: Glutathione; HIF-1α: Hypoxia-inducible factor-1 alpha; LIP: Labile iron pool; mTOR: Mammalian target of rapamycin; NCOA4: Nuclear receptor coactivator 4; PI3K: Phosphatidylinositol 3 kinase; RA: Rheumatoid arthritis; SAM: S-adenosylmethionine; SCD-1: Stearoyl-CoA desaturase 1; SLC3A2: Solute carrier family 3 member 2; SLC7A11: Solute carrier family 7 member 11; SREBP1: Sterol-regulatory element binding protein 1; TNF: Tumor necrosis factor.